ArticleCellular microbiology2013
Regulation of Toll-like receptor 2 interaction with Ecgp96 controls Escherichia coli K1 invasion of brain endothelial cells.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Deciphering defensive mechanisms inFrontiers in immunology · 2026Review
- Endotoxin-Free Outer Membrane Vesicles for Safe and Modular Anticancer Immunotherapy.ACS synthetic biology · 2025Article
- Dual role of TLR4 in bacterial meningitis through regulating endothelial pyroptosis and inflammatory response during extraintestinal pathogenicFrontiers in immunology · 2025Article
- Article
- GP96 Drives Exacerbation of Secondary Bacterial Pneumonia following Influenza A Virus Infection.mBio · 2021Article
- The shaping of immunological responses through natural selection after the Roma Diaspora.Scientific reports · 2020Article
- Lipid rafts and pathogens: the art of deception and exploitation.Journal of lipid research · 2020Review
- Article
- Escherichia coli K1 Modulates Peroxisome Proliferator-Activated Receptor γ and Glucose Transporter 1 at the Blood-Brain Barrier in Neonatal Meningitis.The Journal of infectious diseases · 2016Article
- Host-pathogen interactions in bacterial meningitis.Acta neuropathologica · 2016Review
- Pertussis Toxin Exploits Specific Host Cell Signaling Pathways for Promoting Invasion and Translocation of Escherichia coli K1 RS218 in Human Brain-derived Microvascular Endothelial Cells.The Journal of biological chemistry · 2015Article
- Identification of minimum carbohydrate moiety in N-glycosylation sites of brain endothelial cell glycoprotein 96 for interaction with Escherichia coli K1 outer membrane protein A.Microbes and infection · 2014Article
- Angiotensin II receptor type 1--a novel target for preventing neonatal meningitis in mice by Escherichia coli K1.The Journal of infectious diseases · 2014Article
- Resistance of the brain to Escherichia coli K1 infection depends on MyD88 signaling and the contribution of neutrophils and monocytes.Infection and immunity · 2013Article
- Listeria monocytogenes triggers the cell surface expression of Gp96 protein and interacts with its N terminus to support cellular infection.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The interaction of outer membrane protein A (OmpA) with its receptor, Ecgp96 (a homologue of Hsp90β), is critical for the pathogenesis of Escherichia coli K1 meningitis. Since Hsp90 chaperones Toll-like receptors (TLRs), we examined the role of TLRs in E. coli K1 infection. Herein, we show that newborn TLR2(-/-) mice are resistant to E. coli K1 meningitis, while TLR4(-/-) mice succumb to infection sooner. In vitro, OmpA+ E. coli infection selectively upregulates Ecgp96 and TLR2 in human brain microvascular endothelial cells (HBMEC), whereas OmpA- E. coli upregulates TLR4 in these cells. Furthermore, infection with OmpA+ E. coli causes Ecgp96 and TLR2 translocate to the plasma membrane of HBMEC as a complex. Immunoprecipitation studies of the plasma membrane fractions from infected HBMEC reveal that the C termini of Ecgp96 and TLR2 are critical for OmpA+ E. coli invasion. Knockdown of TLR2 using siRNA results in inefficient membrane translocation of Ecgp96 and significantly reduces invasion. In addition, the interaction of Ecgp96 andTLR2 induces a bipartite signal, one from Ecgp96 through PKC-α while the other from TLR2 through MyD88, ERK1/2 and NF-κB. This bipartite signal ultimately culminates in the efficient production of NO, which in turn promotes E. coli K1 invasion of HBMEC.
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